河豚毒素停搏液对缺血／再灌注心肌细胞钠超载的影响

目的：观察Na^＋通道阻滞剂河豚毒素（TTX）极化心脏停搏液对离体大鼠心肌细胞内游离Na^＋浓度（Na^＋]i）的影响。方法：成年Wistar大鼠心脏,用酶解法分离成具有搏动性的单个心室肌细胞悬液,随机分成基础组、STH2组（缺血／再灌注损伤对照组）和TTX组（实验组）,STH2组和TTX组分别应用St．ThomasⅡ号停搏液和TTX停搏液处理,建立模拟缺血／再灌注损伤的停搏／复搏细胞模型,激光扫描共聚焦显微镜（LSCM）测定各组细胞不同时期的Na^＋]。倒置显微镜观察细胞形态学变化。结果：TTX组和STH2组细胞复搏后Na^＋];均明显高于基础组（P〈0．01）,但TTX组明显低于STH2组（P〈0．01）;在停搏期间,TTX组细胞Na^＋]i上升速度和幅度明显低于STH2组;形态学观察,TTX组复搏后具有正常活力的杆形心肌细胞比例高于STH2组（P〈0．01）。结论：河豚毒素心脏停搏液较去极化心脏停搏液能减轻心肌细胞Na^＋超载和缺血／再灌注损伤。

Effects of cardioplegia with tetrodotoxin on intracellular sodium overload of ischemia/reperfusion cardiomyocytes

Aim： To investigate the effects of polarizing cardioplegia solution with sodiumchannel inhibitor tetrodotoxin（TTX） on intracellular free Na^＋ concentration（ Na^＋ ]i） in isolated cardiomyocytes of rat. Methods： Ventricular myocytes with beating were isolated from adult rat hearts by enzymatic dissociation, randomly created in group base, group STH2（contrast group of ischemia/reperfusion） and group TTX（treated group）. Both Group STH2 and group TTX were arrested by St. Thonms No. 2 cmvlioplegia solution and TTX cardioplegia solution respectively, the arrest/re-beating cell model imitating MIRI being established, and imagcd by laser scanning colffocal microscopy（LSCM） for measuring Na^＋]i of cardiomyocytes in different period. The morphology of cardiomyocytes was observed under the inverted microscope. Results： Na^＋ ]i of cardiomyocytes in both group TTX and group STH2 after re-beating was higher than that in group base（ P 〈 0.01）, and Na^＋ ]i in group TTX was lower than that in group STH2（ P 〈 0.01）. During arrest, the elevation of Na^＋]i in group TTX was lower than that in group STH2. During arrest, the elevation ofNa^＋ ]i in group TTX was lower than that in group STH2. Morphologically, after re-beating, the ratio of active cardiomyocytes with normal form in group TTX was higher than that in group STH2（ P 〈 0.01）. Conclusion： Contrast depolarized cardioplegia solution, TTX cardioplegia solution could alleviate ischemia reperfusion injury and intracel lular Na^＋ overload of cardiomyocytes.